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Peter H. Krammer

Researcher at German Cancer Research Center

Publications -  473
Citations -  69037

Peter H. Krammer is an academic researcher from German Cancer Research Center. The author has contributed to research in topics: Fas receptor & Apoptosis. The author has an hindex of 125, co-authored 472 publications receiving 66945 citations. Previous affiliations of Peter H. Krammer include University of Texas Southwestern Medical Center & Boston Children's Hospital.

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FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death--inducing signaling complex.

TL;DR: This work utilized nano-electrospray tandem mass spectrometry to identify CAP3 and CAP4, components of the CD95 (Fas/APO-1) death-inducing signaling complex, and found a novel 55 kDa protein, designated FLICE, which has homology to both FADD and the ICE/CED-3 family of cysteine proteases.
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Two CD95 (APO-1/Fas) signaling pathways

TL;DR: In the presence of caspase‐3 the amount of active casp enzyme‐8 generated at the DISC determines whether a mitochondria‐independent apoptosis pathway is used (type I cells) or not (type II cells).
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Cytotoxicity-dependent APO-1 (Fas/CD95)-associated proteins form a death-inducing signaling complex (DISC) with the receptor.

TL;DR: The data suggest that in vivo CAP1–4 are the APO‐1 apoptosis‐transducing molecules.
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Death and anti-death: tumour resistance to apoptosis

TL;DR: What are the molecular mechanisms of tumour resistance to apoptosis and how can the authors use this knowledge to resensitize tumour cells to cancer therapy?
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Monoclonal antibody-mediated tumor regression by induction of apoptosis

TL;DR: Histological thin sections of the regressing tumor showed that anti-APO-1 was able to induce apoptosis in vivo, suggesting induction of apoptosis as a consequence of a signal mediated through cell surface molecules like APO- 1 may be a useful therapeutic approach in treatment of malignancy.